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DOI: 10.5498/wjp.v5.i1.103
Postpartum depression: A systematic review of the genetics
involved
Tiago Castro e Couto, Mayra Yara Martins Brancaglion, António Alvim-Soares, Lafaiete Moreira,
Frederico Duarte Garcia, Rodrigo Nicolato, Regina Amélia Lopes P Aguiar, Henrique Vitor Leite,
Humberto Corrêa
Tiago Castro e Couto, Mayra Yara Martins Brancaglion,
António Alvim-Soares, Lafaiete Moreira, Frederico Duarte
Garcia, Rodrigo Nicolato, Humberto Corrêa, Postgraduate
Program in Molecular Medicine, School of Medicine, Universidade
Federal de Minas Gerais ,Belo Horizonte 30130100, MG, Brazil
Regina Amélia Lopes P Aguiar, Henrique Vitor Leite, Department
of Obstetrics and Gynecology, School of Medicine, Universidade
Federal de Minas Gerais, Belo Horizonte 30130100, MG, Brazil
Frederico Duarte Garcia, Humberto Corrêa, Department of
Mental Health, School of Medicine, Universidade Federal de
Minas Gerais, Belo Horizonte 30130100, MG, Brazil
Author contributions: All authors equally contributed to this paper.
Supported by Humberto Corrêa has received research funding
from Fundação de Amparo à Pesquisa do Estado de Minas
Gerais (FAPEMIG) and Conselho Nacional de Desenvolvimento
Científico e Tecnológico (CNPq).
Conflict-of-interest: The others authors have no conflicts-of-
interest or received any grant.
Open-Access: This article is an open-access article which was
selected by an in-house editor and fully peer-reviewed by external
reviewers. It is distributed in accordance with the Creative
Commons Attribution Non Commercial (CC BY-NC 4.0) license,
which permits others to distribute, remix, adapt, build upon this
work non-commercially, and license their derivative works on
different terms, provided the original work is properly cited and
the use is non-commercial. See: http://creativecommons.org/
licenses/by-nc/4.0/
Correspondence to: Tiago Castro e Couto, MD, Postgraduate
Program in Molecular Medicine, School of Medicine, Universidade
Federal de Minas Gerais, Alfredo Balena Av, 190/240 Santa Efigênia,
Belo Horizonte 30130100, MG,
Brazil. tiagocastrocouto@gmail.com
Telephone: +55-31-34099785
Fax: +55-34-32242884
Received: July 17, 20114
Peer-review started: July 19, 20114
First decision: October 14, 2014
Revised: November 21, 2014
Accepted: December 16, 2014
Article in press: December 17, 2014
Published online: March 22, 2015
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World J Psychiatr 2015 March 22; 5(1): 103-111
ISSN 2220-3206 (online)
© 2015 Baishideng Publishing Group Inc. All rights reserved.
REVIEW
Abstract
Postpartum depression is one of the most prevalent
psychopathologies. Its prevalence is estimated to be
between 10% and 15%. Despite its multifactorial
etiology, it is known that genetics play an important
role in the genesis of this disorder. This paper reviews
epidemiological evidence supporting the role of genetics
in postpartum depression (PPD). The main objectives
of this review are to determine which genes and
polymorphisms are associated with PPD and discuss
how this association may occur. In addition, this paper
explores whether these genes are somehow related to
or even the same as those linked to Major Depression
(MD). To identify gaps in the current knowledge that
require investigation, a systematic review was conducted
in the electronic databases PubMed, LILACS and SciELO
using the index terms “postpartum depression” and
“genetics”. Literature searches for articles in peer-
reviewed journals were made until April 2014. PPD was
indexed 56 times with genetics. The inclusion criteria
were articles in Portuguese, Spanish or English that
were available by institutional means or sent by authors
upon request; this search resulted in 20 papers. Genes
and polymorphisms traditionally related to MD, which
are those involved in the serotonin, catecholamine,
brain-derived neurotrophic factor and tryptophan
metabolism, have been the most studied, and some
have been related to PPD. The results are conflicting
and some depend on epigenetics, which makes the data
incipient. Further studies are required to determine the
genes that are involved in PPD and establish the nature
of the relationship between these genes and PPD.
Key words: Genetics; Single nucleotide polymorphisms;
Molecular; Postpartum depression; Genes
© The Author(s) 2015. Published by Baishideng Publishing
103 March 22, 2015|Volume 5|Issue 1|
 Couto TC et al . Postpartum depression: A systematic review
Group Inc. All rights reserved.
Core tip: 5HTT and 5HTTLPR were the most studied
gene and polymorphism, respectively. 5HTTLPR is
associated with postpartum depression (PPD) in the
majority of papers, but epigenetics must be considered.
TPH1 and TPH2 polymorphisms are related to peripartum
depression. COMT and MAOA polymorphisms were also
risk factors for PPD. Once again, only when epigenetic
was analyzed, an association with BDNF polymorphism
was possible. MTHFR, CYP2D6 and PER2 polymorphisms
were not related to this mood disorder. Polymorphisms
of oxytocin, steroids and estrogen genes were positively
correlated with PPD.
Couto TC, Brancaglion MYM, Alvim-Soares A, Moreira L, Gar-
cia FD, Nicolato R, Aguiar RAL, Leite HV, Corrêa H. Postpartum
depression: A systematic review of the genetics involved. World J
Psychiatr 2015; 5(1): 103-111 Available from: URL: http://www.
wjgnet.com/2220-3206/full/v5/i1/103.htm DOI: http://dx.doi.
org/10.5498/wjp.v5.i1.103
INTRODUCTION
Historically, pregnancy and puerperium have been
considered periods that protect women from mental
disorders. It is now known that the opposite is true:
those periods confer a higher risk of appearance and
recurrence of mental disorders and should therefore
be a public health concern. Postpartum depression
(PPD) is one of these disorders. Epidemiological papers
demonstrated that the prevalence of postpartum
[1-3]
depression is between 10% and 15% .
The adverse impacts of PPD are not limited to
mothers; PPD also affects other family members
and influences family dynamics. Recent studies have
shown that PPD can also lead to significant language,
cognitive and emotional processing problems in
[4-6]
children . Psychopathologies in children may not be
restricted to the first years of life; it is possible to find
manifestations, such as conduct disorder, that persist
[7]
even until adolescence . The partners of women with
PPD also tend to have depression more frequently than
expected .
[8,9]
Psychological and social changes mark the transition
to motherhood. Those changes, together with clinical
history and obstetrical aspects, may be related to PPD.
Self-esteem, childcare stress, life stress, social support,
marital relationship, infant temperament, marital
status, socioeconomic status, unplanned/unwanted
[10]
pregnancy , previous psychiatric disorder
[1,10]
, method
of childbirth, and previous abortion
[11]
are the main
findings associated with PPD.
In addition, biological changes are related to PPD.
According to some investigations, these changes may
be partly genetically determined. A study conducted in
England evaluated 44 pairs of sisters who had unipolar
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depression and found that those pairs in which one
sister fulfilled the PPD criteria according to DSM-Ⅳ,
42% of the other sisters developed PPD after giving
birth. For those who had no family history of depression,
the rates dropped to 15% (P = 0.01). In this study,
the evidence of a genetic influence is even greater
when the PPD period was restricted for 6 to 8 wk
[12]
postpartum . Another study, conducted in Australia,
involved the interview of 838 pairs of adult twins about
their postpartum experiences. The authors reported
that genetic factors explained 25% of the variance in
[13]
the occurrence of PPD . Over the last decade, many
studies have been devoted to verifying the impact
of this type of genetic variation in PPD, and it is thus
important to know the concept of Single Nucleotide
Polymorphisms (SNPs). SNP is a genetic variation
that affects only one base pair in the DNA sequence.
These variations in DNA sequence can affect the
individual response to diseases, bacteria, viruses,
chemicals, pharmaceuticals. To be considered an
SNP, the variation should occur in at least 1% of a
given population.
The present report aims to assess molecular
studies associated with PPD and highlight the
most studied genes and polymorphisms.
RESEARCH
The present paper is a systematic, integrative review that
includes several studies with different methodologies
to answer questions about the relationship between
genetic factors and the development of postpartum
depression. For guidance, the following questions were
raised: Are there genes or polymorphisms that are
more related than others to postpartum depression?
What is their relevance? Are Major Depression (MD) and
Postpartum Depression the same or different disorders?
Is PPD only a temporal variant of MD?
This study consisted of a search of all articles
describing a clear relationship between genetics and
postpartum depression that were indexed in PubMed,
LILACS and SciELO published before April 2014.
To accurately answer the questions that guided this
review, the abstracts were read and classified during a
selection process. If, after reading the abstract, there
was reasonable doubt about the inclusion or exclusion
of the paper, the whole article was read. The same
procedure was adopted when abstracts were not
available. Thereafter, a reverse search was carried out.
The following inclusion and exclusion criteria were
used.
Included: papers in Portuguese, Spanish or English in
the researched databases, with index terms “postpartum
depression” and “genetics”, which assessed the genes
and polymorphisms related to PPD. For this purpose,
the following algorithms were used: (“Depression,
Postpartum”[Mesh]) AND (“Genetics”[Mesh] OR
“genetics”[Subheading]).
104 March 22, 2015|Volume 5|Issue 1|
 Couto TC et al . Postpartum depression: A systematic review

Excluded: review articles and animal models; chromosomes 1 and 9 by Genome-Wide Association
[64]
articles that were not available by CAPES (Brazilian Studies (GWAS) .
governmental agency that sponsors studies) and The most studied polymorphism was the 5-HTTLPR,
[48-50,52,56-58,66]
not provided by authors upon request; those that which was addressed in eight articles ; some
researched another postpartum psychopathology, of these articles also analyzed other polymorphisms in
[57,58] [51]
finding or result; and those that did not address the 5HTT, such as STin2 VNTR and rs140700 .
genetics involved in PPD. The remaining studied polymorphisms were those
[55,60,61,66] [48,52,62,66] [48,52,66]
of TPH 1 and 2 , COMT , MAO ,
[47,50] [53] [54] [50]
BDNF , CYP2D6 , MTHFR , Per 2 , OXT/OXTR
RESULTS [63] [65]
genes and GR/CRHR1 genes . Pinssoneault et al
[66]

The LILACS and SciELO searches did not result in adopted a different strategy: in addition to looking
any article fulfilling the criteria. The PubMed search for polymorphisms of the estrogen receptor alpha
resulted in 56 papers. After reading the abstracts, 36 gene (ESR1), they looked for associations with the
[14-19]
were excluded: 6 reviews , 2 papers that were not polymorphisms already cited in this report (MAOA,
available by CAPES and not sent by the authors upon COMT, TPH2, 5HTTLPR SNPs) besides those of the
[20,21] [22-26] [66] [59]
request , 5 animal models , 12 investigating genes HTR2A, DAT and DRD2 . Segman et al used
another postpartum psychopathology (psychoses and a different approach, analyzing not polymorphisms but
[27-38] [6,39,40] [64]
bipolar) , 3 evaluating the children , 1 on 3142 active transcripts, whereas Mahon et al studied
[41]
breastfeeding and 7 that did not address the genetic 16.916 SNPs through GWAS (Table 1).
[12,13,42-46]
factors involved in PPD . A reverse search
resulted in no additional items. Finally, a sample was
formed
[47-66]
. DISCUSSION
The 20 selected studies were conducted in 10 The data regarding 5HTT gene polymorphisms were
[48,50,53] [52]
different countries. Sweden and the United variable. Doornbos et al performed the only study
[49,57,64]
States of America had three publications each that found an independent relationship between PPD
[56,61] [55,60] [51,58]
(15%). Germany , China (Taiwan) , Spain , and the 5HTTLPR polymorphism whereby subjects
[63,66] [54,65] [47,62]
Canada , the United Kingdom and Brazil had with the 5HTTLPR long allele variable developed PPD.
[59] [52] [49] [58]
two papers each (10%). Israel and Netherlands had Binder et al and Sanjuan et al found a significant
one paper (5%) each (Table 1). association between 5HTTLPR and PPD only at 8 wk
Of the selected sample, the 5HTT gene was the most postpartum, but the results became nonsignificant in
[48-50,52,56-58,66]
studied . Genes associated with tryptophan a posteriori analysis, suggesting that the findings were
[55,60,61,66]
metabolism and Catechol-O-methyl transferase dependent on the evaluation time point. The remaining
[48,52,62,66]
(COMT) were the next most researched. 5HTTLPR studies also depended on covariates to
Monoamine Oxidase (MAO) gene was studied in three achieve statistically significant associations with PPD:
[48,52,66] [57]
of the articles included in this review , and the unfavorable environments ; previous psychiatric
Brain-Derived Neurotrophic Factor (BDNF) gene was history, maternity stressors and COMT-Val158Met
[47,50] [48] [50]
studied in two articles . Two articles analyzed allele ; autumn or winter delivery ; stressful life
[56]
genes that are not commonly evaluated in depression events ; and a gene-gene interaction with ESR1 TA
[66]
studies: the Methylenetetrahydrofolate Reductase repeat .
[54] [53]
(MTHFR) gene and the CYP2D6 gene . One article The TPH gene study showed a significant difference
[50]
was about circadian gene Per 2 , and one was about in genotype frequency for the T27224C polymorphism
the oxytocin gene (OXT) and oxytocin receptor gene between standard groups and those with comorbid
[63] [51]
(OXTR) . Costas et al assessed 44 genes involved in depression and anxiety, with risk analysis showing that
pathways that are hypothetically related to the etiology the C allele conferred a strong protective effect for
of postpartum mood disorders, that is, those included depression and anxiety. This finding suggests that the
in the HPA axis, in the effects of stress in the prefrontal TPH1 gene has an important role in the pathogenesis
[60]
cortex, and in the regulation of sex hormones. Looking of postpartum mental disorders . Similarly, one
for an association between PPD and the HPA axis, of the TPH2 gene studies attested that the C2755A
[65]
Engineer et al tested the glucocorticoid (GR) and polymorphism could be considered a risk factor for
type 1 corticotropin-releasing hormone (CRHR1) depression. The C2755A polymorphism occurred
receptor genes. Based on the results of Costas’ paper, only in women with peripartum major depression
[66]
Pinssoneault et al researched the ESR1 gene both and anxiety disorders (P = 0.043) and exhibited a
as a principal outcome and under the additive power dominant gene action (P = 0.038) with an estimated
of other genes: COMT, TPH2, MAOA, 5HTT, dopamine disease risk of 1.73. Hence, despite its small sample
receptor D2 (DRD2), serotonin receptor 2A (HTR2A) size, this study suggests that TPH2 represent a
and dopamine transporter (DAT). An Israeli study population-specific risk factor for peripartum major
[55]
evaluated peripheral blood mononuclear cell (PBMC) depression . A recent study supports that conclusion;
[59]
gene expression . Finally, an American study analyzed it found that a haplotype block in the promoter
417 microsatellite markers in linkage studies and region of TPH2 showed significant associations with

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 Table 1 Genes and polymorphisms associated with postpartum depression

Article Ref. Country Instrument Genes Polymorphisms

CYP2D6 genotypes and depressive symptoms during Josefsson et Sweden EPDS CYP2D6 CYP2D6*1 (wild type), CYP2D6*3, CYP2D6*4
late pregnancy and postpartum al[53]
Association of tryptophan hydroxylase gene Sun et al[60] China SADS TPH1 T3840A, A12517C, A20004C, G347T, T27224C
polymorphism with depression, anxiety and comorbid
depression and anxiety in a population-based sample of
postpartum Taiwanese women
Mood changes after delivery: role of the serotonin Sanjuan et Spain EPDS/DIGS 5HTT 5HTTLPR, STin2 VNTR
transporter gene al[58]
The development of peripartum depressive symptoms Doornbos et Netherland EPDS MAOA, 5HTT, COMT MAOA , 5HTTLPR, COMT Val158Met

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is associated with gene polymorphisms of MAOA, al[52]
5-HTT and COMT
Population-specific functional variant of the TPH2 gene Lin et al[55] China SADS TPH2 T-703G, T-473A, A90G, C2755A, C10662T, G93329A
2755C>A polymorphism contributes risk association to
major depression and anxiety in Chinese peripartum
women
Genome-wide linkage and follow-up association study Mahon et United States DIGS 417 microsatellite markers in linkage studies / 16.916
of postpartum mood symptoms al[64] SNPs in the 1 and 9 chromosomes for GWAS.
Blood mononuclear cell gene expression signature of Segman et Israel EPDS PBMC gene expression 3142 active transcripts set
postpartum depression al[59]
A serotonin transporter gene polymorphism predicts Binder et al[49] United States SCID/ 5HTT 5HTTLPR

106
Couto TC et al . Postpartum depression: A systematic review

peripartum depressive symptoms in an at-risk HRSD-17

psychiatric cohort
Association study of 44 candidate genes with depressive Costas et al[51] Spain EPDS/DIGS 44 genes involved in pathways hipothetically related to the 388 SNPs
and anxiety symptoms in post-partum women etiology of postpartum mood disorders: HPA axis, effects of
stress in the prefrontal cortex, and regulation of sex hormones
An association study between the Val66Met Figueira et Brazil EPDS BDNF BDNF Val66Met
polymorphism of the BDNF gene and postpartum al[47]
depression
Postpartum depression symptoms: a case-control study Comasco et Sweden EPDS COMT, MAOA, 5HTT COMT Val158Met, MAOA uVTNR, 5HTTLPR.
on monoaminergic functional polymorphisms and al[50]
environmental stressors
Role of mother’s genes and environment in postpartum Mitchell et United States CIDI-SF 5HTT 5HTTLPR , STin2 VNTR
depression al[57]
Postpartum depressive symptoms and the BDNF Comasco et Sweden EPDS BDNF, 5HTT, PER2 BDNF Val66Met, PER2 SNP 10870 (G and A), 5HTTPLR (L
Val66Met functional polymorphism: effect of season of al[50] and S)
delivery
Folic acid supplementation during pregnancy may Lewis et al[54] England EPDS MTHFR C677T
protect against depression 21 months after pregnancy,
an effect modified by MTHFR C677T genotype
The 5-HTTLPR polymorphism modulates the influence Mehta et al[56] Germany EPDS 5HTT 5HTTLPR
on environmental stressors on peripartum depression
symptoms

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 Genetic variants in the tryptophan hydroxylase 2 gene Fasching et Germany EPDS TPH2 rs11178993, rs6582071, rs11178997, rs7955501, rs17110536,
(TPH2) and depression during and after pregnancy al[61] rs4760814, rs7300641, rs4760820, rs10879354, rs1487275,
rs10879358, rs11615016, rs17110747, rs1872824
Postpartum depression symptoms associated with Alvim- Brazil EPDS COMT COMT Val158Met
Val158Met COMT polymorphism Soares et al[62]
Interaction between oxytocin genotypes and early Mileva-Seitz Canada CES-D OXT, OXTR OXT: rs2740210, rs4813627/ OXTR: rs237885
experience predicts quality of mothering and et al[63]
postpartum mood
Association of glucocorticoid and type 1 corticotropin- Engineer et United EPDS GR, CRHR1 GR: BclI, ER22/23EK/CRHR1: s1876828, rs242939,
releasing hormone receptors gene variants and risk for al[65] Kingdom rs242941
depression during pregnancy and post-partum
Association study of the estrogen receptor gene ESR1 Pinsonneault Canada MINI, SCID, ESR1, COMT, TPH2, DRD2, HTR2A, DAT, MAOA, 5HTT ESR1: TA repeat, rs2077647, rs1801132, rs3798577,
with postpartum depression - a pilot study et al[66] EPDS and/or rs988328, rs1884051, rs3020327, rs9340958, rs3020434/

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MADRS HTR2A: rs6314, rs6311/DAT: rs27072, rs6347, In8VNTR/
5HTTLPR/MAOA: rs1137070, pVNTR/TPH2: rs7305115 /
DRD2: rs2283265 / COMT: rs4680

EPDS: Edinburgh Postnatal Depression Scale; SADS: Schedule for Affective Disorders and Schizophrenia; DIGS: Diagnostic Interview for Genetics Studies; SCID: Structured Clinical Interview for DSM-IV; HRSD-17: 17-item
Hamilton Rating Scale for Depression; CIDI-SF: Composite International Diagnostic Interview-short form; CES-D: Center for Epidemiological Studies Depression Scale; MADRS: Montgomery-Asberg Depression Scale; TPH:
Tryptophan hydroxylase; 5HTT: Serotonin transporter; MAOA: Monoamine oxidase A; COMT: Catechol-O-methyltransferase; PBMC: Peripheral blood mononuclear cell; BDNF: Brain-derived neurotrophic factor; PER2: Period
circadian clock 2; MTHFR: Methylenetetrahydrofolate reductase; OXT: Oxytocin; OXTR: Oxytocin receptor; GR: Glucocorticoid receptor; CRHR1: Type 1 corticotropin-releasing hormone receptor; ESR1: Estrogen receptor alpha;
DRD2: Dopamine receptor D2; HTR2A: Serotonin receptor 2A; DAT: Dopamine transporter.

107
[61]
depression values during pregnancy and 6-8 mo after pregnancy . This last paper also showed that the SNP rs10879354 had a significant association with depression
[66]
throughout the postpartum period. A gene-gene interaction with ESR1 gene was not found .
[48,52,62,66] [48,52,66]
Four papers focused on the COMT genes , with three of them also focusing on the MAOA gene . COMT-Val158Met allele polymorphism was one of the
[48,52,62] [48,52,66]
main risk factors for PPD , despite not being an independent risk factor . Previous psychiatric contact, maternity stressors and the time of the evaluation
[48]
(6 wk or 6 mo postpartum) influenced the relationship . Similarly, the interaction with MAOA - L polymorphism was associated with more pronounced depressive
[52]
symptoms than when the COMT-Val158 Met allele was considered alone . MAOA rs1137070 and COMT rs4680 polymorphisms were found to have an additive effect
[66]
plus ESR1 in producing PPD .
[47] [50]
Figueira et al and Comasco et al did not find any linear correlation between PPD and the BDNF ValMet polymorphism. The correlation showed a trend toward
[47,50] [50]
significance among Met allele carriers . There was a cumulative and significant effect of the presence of Met allele and autumn/winter delivery .
The C677T polymorphism was also studied in a study that focused on the association between MTHFR and PPD. Its results indicated that low folate levels do not
appear to be a significant risk factor for peripartum depression but may be a factor for non-gestational-related depression, especially in women with the MTHFR C677T
[54]
TT genotype . The study on CYP2D6 showed that in a sample that included 45 women reporting symptoms of depression only during pregnancy, 56 women reporting
symptoms of depression only after pregnancy and 44 women reporting symptoms of depression both during and after pregnancy, there were no differences in CYP2D6
[53]
genotyping and depressive symptoms .
Circadian genes did not appear to have a “family“ effect. Despite the correlation between postpartum depressive onset in bipolar disorder and Per3 4/4
[37] [50]
homozygotes , the circadian gene Per 2 was not related to PPD .
[67]
As in Major Depression , the OXTR gene appears to be related to perinatal depression. Its SNP rs237885 was associated with pre-natal, but not post-natal,
[63]
depression scores . There was also a correlation between OXT SNPs rs2740210 and rs4813627 and depression score 6 mo after delivery. However, this finding seems
Couto TC et al . Postpartum depression: A systematic review

to be mediated by mother’s early life quality of care because the association was not retained in the regression model. That is, these appear to be separate effects

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 Couto TC et al . Postpartum depression: A systematic review
[63]
rather than causally linked outcomes .
[51]
Costas et al studied 44 genes that are hypoth­
etically linked to depression and, after correcting for
multiple tests, did not find a significant relation between
any of the SNPs tested and PPD. Nevertheless, a
post hoc analysis showed that a combination of three
SNPs of the protein kinase C beta gene (PRKCB):
rs198183, rs381901 and rs2051684, achieved statistical
[51]
significance (global P = 0.0001596) , turning it into a
potential target.
The GR polymorphism BclI, but not the ER22/23EK,
showed a positive association with high EPDS score
and, therefore, PPD. This correlation was also positive
for the minor allele rs242939 SNP of the CRHR1 gene,
with the particularity that a relation with prenatal
[65]
EPDS score could also be found in this case . This
result supports Brummelte and Galea’s statement that
there are changes in all aspects of the HPA system
(ACTH, CRH and cortisol) during pregnancy and the
postpartum period. Women who are susceptible to
HPA axis dysregulation may be particularly vulnerable
[68]
for developing stress-related disorders at this time .
Two variants in the ESR1 gene, the TA repeat and
rs2077647, were statistically associated with EPDS
[66]
scores and PPD , suggesting that estrogen-linked
molecular mechanisms could also be involved in PPD
genesis. Conversely, gene-gene interactions detected
with encoding serotonergic signaling proteins (5HTT
and HTR2A) reinforce serotonin’s contribution to PPD.
[59]
Segman et al , analyzing PBMC gene expression
and its 3142 active transcripts, found a signature
of 73 active transcripts showing 1.5-fold or higher
significant association with PPD. Of those, a subsample
of 57 transcripts remained significant in the secondary
analysis. Despite the small sample size of the study,
both the 73 and 57 differential transcript sets (but not
the 3142) correctly distinguished PPD patients from
controls. This capability could be used as a prognostic
tool, allowing for the initial screening of mothers who
are at higher risk for PPD development.
[64]
Finally, Mahon et al used linkage and GWAS
techniques and found that the chromosomes 1q21.3-
­q32.1 and 9p24.3p22.3 were associated with postpartum
depressive mood. The authors suggest that Hemicentin
1 (HMCN1) and Methyltransferase like 13 (METTL13)
genes on chromosome 1 contain polymorphisms that
confer vulnerability for PPD, highlighting the notion that
specific studies of those genes should be attempted .
[64]
These results must be watched with caution because
bipolar patients with postpartum depressive onset were
mingled in the sample. However, a study published last
month also confirmed that an HMCN1 polymorphism
(rs2891230) is associated with PPD diagnosis in a
[69]
population without bipolar diagnosis .
Despite the substantial number of genes and
polymorphisms reviewed here, there are still others that
[24]
need testing. For instance, Maguire et al noticed a
relationship between GABAA receptor plasticity during
pregnancy and PPD and proposed an animal model
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using GABAAR δ subunit deficient mice. Therefore,
[24]
GABAergic genes may also be potential targets .
Another important genetic mechanism involved in
Major Depression and not tested in PPD studies is the
course of inflammation genes. Because functional allelic
variants of the genes for IL-1b and TNF-a increase the
risk for depression and are associated with reduced
[70-72]
responsiveness to antidepressant therapy , their
influence under PPD would be interesting to measure.
Overall, all of the articles selected had large sample
sizes, thus rendering reliable results. Some of the
differences found for the same polymorphism may be
attributed to different methods used for PPD diagnosis,
as observed in table 1. Another important point to note
is that it seems, as in other psychiatric disorders, that
genetic influence appears not to be sufficient by itself
to cause the disorder. The development of psychiatric
disorders is often dependent on epigenetics, and
an environmental trigger is often required for these
[48,50,57]
diseases to develop .
[73]
Riecher-Rössler et al stated that there is no
doubt that sex and gender, with their biological and
psychosocial correlates, strongly affect mental health,
given the marked difference regarding the prevalence,
symptoms, risk factors and outcomes of psychiatric
disorders between the sexes. Nevertheless, using
PPD as an example, the author shows that such
influence is necessary to ensure better clinical care
and not to justify the existence of a distinct diagnostic
entity. It was possible to demonstrate that the factors
used to define “true” or “valid” psychiatric disorders:
descriptive validity (the same symptoms), construct
validity (the same risk factors) and predictive validity
[73]
(the same course) are not satisfied in PPD . MD and
PPD apparently share the same genetic background
because PPD seems to be linked to MAO, COMT,
5HTT and other pathways usually related to MD. In
our opinion, this strengthens the possibility that they
[74,75]
are the same disorder with a temporal variant .
However, there are not sufficient published data to
determine whether there is a specific etiological factor
that is capable of differentiating those two disorders.
Further studies are needed to nullify this hypothesis,
and for that, other candidate genes must also be
researched.
CONCLUSION
This review summarizes the representative findings
in the literature regarding the genetics involved in
Postpartum Depression.
The main conclusion of this review is that similar
genes tend to be studied in Postpartum Depression and
that these genes have a similar pattern to those already
associated with Major Depression in the literature.
The relationship between molecular genetics and
PPD is an extremely current issue. The oldest article
selected was from 2004, and the newest was from
2013. However, there is still little research in this area
108 March 22, 2015|Volume 5|Issue 1|

compared with other psychiatric disorders, and it
deserves further study due to its importance in terms
of public health.
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